ライフサイエンスコーパス: acetylcysteine

1 nit, which was restored in the presence of N-acetylcysteine.

2 88, and oxidative stress was attenuated by N-acetylcysteine.

3 diated relaxations, which were reversed by N-acetylcysteine.

4 ure-dependent tone, which were annulled by N-acetylcysteine.

5 other set of mice received the antioxidant N-acetylcysteine.

6 of LKB1 and by incubation with antioxidant N-acetylcysteine.

7 efect, which is rescued by the antioxidant N-acetylcysteine.

8 edanib, followed by imatinib, dasatinib, and acetylcysteine.

9 the phenotype by the antioxidant action of N-acetylcysteine.

10 ss program were blocked by the antioxidant N-acetylcysteine.

11 and can be prevented with the antioxidant N-acetylcysteine.

12 smid that was prevented by the addition of N-acetylcysteine.

13 ine signaling 3), and antioxidants such as N-acetylcysteine.

14 oxide, and these effects were inhibited by N-acetylcysteine.

15 ubstantially reduced in mice that received N-acetylcysteine.

16 She was treated with N-acetylcysteine.

17 he NOX subunit NOX2 and by the antioxidant N-acetylcysteine.

18 hronic treatment with the cystine prodrug, N-acetylcysteine.

19 clones were cultivated in the presence of N-acetylcysteine.

20 longed therapeutic efficacy as compared to N-acetylcysteine.

21 piratory epithelium integrity with EGTA or N-acetylcysteine.

22 of glutamate, alphaKG, or nucleobases with N-acetylcysteine.

23 ed by capsazepine, and by the antioxidant, N-acetylcysteine.

24 in uterine arteries, which was blocked by N-acetylcysteine.

25 CD4 T cells is improved by the antioxidant N-acetylcysteine.

26 Of the 449 acetaminophen overdoses receiving acetylcysteine, 100 were recruited to the study.

27 The study drugs (acetylcysteine 1200 mg or matching placebo) were adminis

28 N-acetylcysteine (3.3%) decreased biofilm biomass and kill

29 were observed, as well as increased use of N-acetylcysteine (48.9% vs. 69.3% overall; 15.8% vs. 49.4%

30 steamine bitartrate (60 mg/kg per day) and N-acetylcysteine (60 mg/kg per day) and were assessed ever

31 response system to receive concomitant oral acetylcysteine (600 mg, three times daily) or placebo fo

32 studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement dru

33 Supplementation of N-acetylcysteine, a glutathione precursor, conferred a pro

34 cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor.

35 gating, and was attenuated by antioxidant N-acetylcysteine, a known scavenger of acrolein.

36 d (2) use the EAAC1(-/-) mouse to evaluate N-acetylcysteine, a membrane-permeable cysteine pro-drug,

37 We also show that N-acetylcysteine, a widely-used antioxidant, is a poor sub

38 urrent administration of the ROS inhibitor N-acetylcysteine abrogated beta-catenin/HIF pathway activi

39 N-acetylcysteine accelerates amputation stump healing in t

40 rug regimen of prednisone, azathioprine, and acetylcysteine; acetylcysteine alone; or placebo.

41 e toxin, whereas replenishing GSH level by N-acetylcysteine administration or activation of nuclear f

42 Mice in posttreatment were treated with N-acetylcysteine after folic acid.

43 JNK inhibitor SP600125, or the antioxidant N-acetylcysteine alleviated insulin resistance, demonstrat

44 rednisone, azathioprine, and acetylcysteine; acetylcysteine alone; or placebo.

45 duced glutamatergic adaptations by chronic N-acetylcysteine also caused enduring inhibition of cocain

46 Furthermore, the administration of N-acetylcysteine also prevented NF-kappaB activation, neut

47 Oral acetylcysteine (also known as N-acetylcysteine) is used

48 ernative antioxidants (vitamin C, DTT, and N-acetylcysteine) also enhanced the chemotactic activity o

49 Chemical chaperones or the antioxidant N-acetylcysteine ameliorated glucose tolerance and insulin

50 generation, and the unrelated anti-oxidant N-acetylcysteine ameliorates TAC-induced pathology.

51 t study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the c

52 pothesized that a novel thiol antioxidant, N-acetylcysteine amide (NACA), might ameliorate cellular d

53 The potent antioxidant, N-acetylcysteine amide (NACA), reduces the severity of a n

54 N-acetylcysteine amide eye drops were administered beginni

55 1D24G501R mutant animals with antioxidants N-acetylcysteine amide or alpha-tocopherol as indicated by

56 peritoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on p

57 randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-induc

58 nsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, protec

59 ir, and to pretreatment with antioxidants (N-acetylcysteine and ascorbate) and placebo.

60 effects could be reverted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectively.

61 he astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of

62 treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinant

63 Combined treatment with N-acetylcysteine and cyclic guanosine monophosphate signal

64 mainly been assessed in adults and include N-acetylcysteine and dexamethasone.

65 t on oxidative stress and the antioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5 u

66 Conversely, antioxidant chemicals (such asN-acetylcysteine and Mn(III)tetrakis(4-benzoic acid)porphy

67 N-acetylcysteine and phosphoinositide 3-kinase (PI3K) inhi

68 s; 133 and 131 patients were enrolled in the acetylcysteine and placebo groups, respectively.

69 Antioxidant N-acetylcysteine and recombinant ALR (rALR) both inhibited

70 All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution.

71 Additional controls of n-acetylcysteine and sodium pyruvate were implemented to p

72 leptogenesis by a transient treatment with N-acetylcysteine and sulforaphane, which act to increase g

73 Four (7%) patients receiving acetylcysteine and three (5%) receiving placebo disconti

74 for the potential roles of bortezomib and N-acetylcysteine, and explore new therapeutic approaches,

75 erior regenerability by each of ascorbate, N-acetylcysteine, and urate when compared to alpha-TOH.

76 In this work, water-dispersible N-acetylcysteine- and l-cysteine-stabilized palladium nano

77 Intravenous sodium bicarbonate and oral acetylcysteine are widely used to prevent acute kidney i

78 /chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phase.

79 Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerobic conditions i

80 hase peroxidation system containing excess N-acetylcysteine as a stoichiometric thiol reducing agent

81 ras(G12D/+);Trp53(fl/fl) mice with 5E1 and N-acetylcysteine, as a ROS scavenger, decreased tumor DNA

82 suppressor cells, whereas the antioxidant N-acetylcysteine attenuates the inhibitory effects of phen

83 Conclusion: Discontinuing acetylcysteine based on laboratory testing after 12 hour

84 in pre- + posttreatment were treated with N-acetylcysteine before folic acid and after folic acid.

85 e treated with a subcutaneous injection of N-acetylcysteine before the folic acid injection.

86 ylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl

87 INR (1.2 versus 1.2) 20 hours after starting acetylcysteine between groups.

88 In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alpha

89 ed similar antioxidant effects in WT mice: N-acetylcysteine blunted beta3-AR stimulation-induced brow

90 New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and ca

91 rescued by treatment with the antioxidant N-acetylcysteine but not by p53 inactivation.

92 d by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathway

93 It is treated with intravenous acetylcysteine, but the standard regimen is complex and

94 lthough treatable by timely application of N-acetylcysteine, can be fatal.

95 hiols, including cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and human serum albumi

96 N-Acetylcysteine, catalase, and l-N(G)-monomethyl arginine

97 tudy assessed the safety and tolerability of acetylcysteine combined with pirfenidone in patients wit

98 Pre-treatment with N-acetylcysteine completely reversed BSO+AUR-induced cell

99 Treatment with N-acetylcysteine could slow the progression of, but not pr

100 The effectiveness of the only antidote, N-acetylcysteine, declines rapidly after APAP ingestion, l

101 Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citra

102 achieved by infusion of 5% dextrose (during acetylcysteine delivery) or saline (for antiemetic pretr

103 N-Acetylcysteine did not prevent ethanol-induced mortality

104 In this subanalysis, acetylcysteine did not reduce the risk of contrast-induc

105 sorbitol, quenching oxidative stress with N-acetylcysteine did suppress both SG formation and TDP-43

106 AK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS),

107 Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1alpha variation observed

108 N-acetylcysteine, diphenyleneiodonium, and apocynin blocke

109 Treatment with the antioxidant N-acetylcysteine disrupts ROS-induced interaction of Mst1/

110 ed protection in the context of suboptimal N-acetylcysteine dosing.

111 N-acetylcysteine (dosing range, 1200-3000 mg/d) or placebo

112 ability of the equine clinical treatments N-acetylcysteine, EDTA, and hydrogen peroxide to disrupt i

113 otosensitivity occurred more frequently with acetylcysteine (eight [13%] patients) than placebo (one

114 The reducing agent N-acetylcysteine eliminated the effects of selenium on ERK

115 emperatures indicate that the -SH group of N-acetylcysteine enhances the rate of its hydrolysis by a

116 mbined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen specie

117 ess which was prevented by the antioxidant N-acetylcysteine (Eur J Neurosci.

118 ients with diabetes mellitus included in the Acetylcysteine for Contrast-Induced Nephropathy Trial (A

119 t randomized study evaluating the effects of acetylcysteine for the prevention of contrast-induced ac

120 Treatment with N-acetylcysteine from gestation on normalized most neuroch

121 s: pharmacological (rescue with trolox and N-acetylcysteine), genetic (analysis of metal-sensitive an

122 61 were assigned to the acetylcysteine group (60 received study medication and i

123 injury (primary end point) was 13.8% in the acetylcysteine group and 14.7% in the control group (rel

124 difference in the change in FVC between the acetylcysteine group and the placebo group (-0.18 liters

125 were no significant differences between the acetylcysteine group and the placebo group in the rates

126 2) and in 114 of 2495 patients (4.6%) in the acetylcysteine group as compared with 112 of 2498 (4.5%)

127 One case of diarrhoea in the acetylcysteine group was considered severe and related t

128 otrusion, and malignant lung neoplasm in the acetylcysteine group, and aortic aneurysm, contusion, fo

129 ltered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose o

130 Historically, intravenous acetylcysteine has been delivered at a fixed dose and du

131 Acetylcysteine has been suggested as a beneficial treatm

132 treated pregnant rats with the antioxidant N-acetylcysteine improved fetal survival but was deleterio

133 are often steatotic, although addition of N-acetylcysteine improves the quality of the cells obtaine

134 e is controversy regarding the benefits of N-acetylcysteine in acute kidney injury.

135 The NACIAM trial (N-acetylcysteine in Acute Myocardial Infarction) examined

136 ectiveness of Prednisone, Azathioprine and N-Acetylcysteine in Patients with IPF) clinical trial.

137 rgistically with the glutathione precursor N-acetylcysteine in preventing biliatresone-induced injury

138 The salutary effects of N-acetylcysteine in this mouse model provide an impetus fo

139 ipants (31 randomized to placebo and 35 to N-acetylcysteine) included in the analysis, 59 (89%) were

140 Furthermore, N-acetylcysteine increased the levels of peroxiredoxin 3 a

141 y addition of nontoxic copper chelators or N-acetylcysteine, indicating a role for copper and reactiv

142 fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosylation of

143 ive stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10 by

144 The cytoprotective antioxidant N-acetylcysteine inhibited Dp44mT-induced autophagosome sy

145 However, three different N-acetylcysteine interventions neither significantly impro

146 hanism in RYR1-related myopathies and that N-acetylcysteine is a successful treatment modality ex viv

147 ion therapy with cysteamine bitartrate and N-acetylcysteine is associated with delay of isoelectric E

148 bination of oral cysteamine bitartrate and N-acetylcysteine is beneficial for patients with neuronal

149 Oral acetylcysteine (also known as N-acetylcysteine) is used with pirfenidone to treat idiopa

150 agents (eg, riluzole, ketamine, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) eit

151 More importantly, the antioxidant, oral N-acetylcysteine led to amelioration of the muscle atrophy

152 tes, reducing reactive oxygen species with N-acetylcysteine lessened protein aggregation and decrease

153 eatment with the redox-active pharmaceutic N-acetylcysteine lowers gastric mucosal neutrophil infiltr

154 N-acetylcysteine may be protective against DILI while taki

155 Time to acetylcysteine (median 7 hours [interquartile ratio 6,12

156 iously reported that phosphocysteamine and N-acetylcysteine mediate ceroid depletion in cultured cell

157 Timely administration of N-acetylcysteine (N-Ac) prevents the progression of seriou

158 probes after pharmacologic challenges with N-acetylcysteine (NAc) and MK-801.

159 abolished by free radical scavenging with N-acetylcysteine (NAC) and Trolox.

160 ent with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced implant

161 ntly, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha a

162 ng Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.

163 N-acetylcysteine (NAC) has anti-atherosclerotic effect wit

164 The use of N-acetylcysteine (NAC) has been recently proposed as a pot

165 Systemic N-acetylcysteine (NAC) has been shown to restore glutamate

166 N-acetylcysteine (NAC) has been suggested to prevent relap

167 For decades, inhaled N-acetylcysteine (NAC) has been used as a mucolytic to red

168 mbination of prednisone, azathioprine, and N-acetylcysteine (NAC) has been widely used as a treatment

169 found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insu

170 alities were all rescued by treatment with N-acetylcysteine (NAC) in diabetic females during gestatio

171 N-acetylcysteine (NAC) is an antioxidant with reactive oxy

172 N-acetylcysteine (NAC) is an FDA-approved drug that has lo

173 N-acetylcysteine (NAC) is known to promote endothelial cel

174 N-acetylcysteine (NAC) is widely used in patients with par

175 atment with the anti-inflammatory compound N-acetylcysteine (NAC) on placental morphologic features w

176 es, the in vivo effects of the antioxidant N-acetylcysteine (NAC) on two mouse models for NPC1 diseas

177 However, pretreatment with N-acetylcysteine (NAC) protects mouse and rat cells from R

178 N-acetylcysteine (NAC) reduces oxidative damage and increa

179 estigate whether a donor pretreatment with N-acetylcysteine (NAC) reduces the incidence of DGF in adu

180 ment of HMVEC-d cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited KSHV entry,

181 gers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited ROS product

182 ric barrier discharge (DBD) plasma treated N-Acetylcysteine (NAC) solution against planktonic and bio

183 gnificant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLLIP

184 We calibrated and applied an N-acetylcysteine (NAC) thiol reactivity assay as a surroga

185 e efficient reversal by a typical antidote N-acetylcysteine (NAC) treatment of APAP-induced liver inj

186 N-acetylcysteine (NAC) was found to improve transplantatio

187 The antioxidant N-acetylcysteine (NAC) was used to decrease ROS in both in

188 ether with 1 of 4 prophylactic regimes (1) N-acetylcysteine (NAC), (2) sodium bicarbonate (NaHCO3) in

189 as to assess the feasibility of using oral N-acetylcysteine (NAC), a glutamatergic modulator and an a

190 continuous intracerebral administration of N-acetylcysteine (NAC), a ROS inhibitor.

191 Supplementation of N-acetylcysteine (NAC), a scavenger of reactive oxygen spe

192 In rodents, N-acetylcysteine (NAC), a stimulator of the cystine-glutam

193 N-Acetylcysteine (NAC), a strong antioxidant and ROS scave

194 N-acetylcysteine (NAC), a thiol-containing antioxidant, ac

195 aim of this study was to determine whether N-acetylcysteine (NAC), an anti-inflammatory antioxidant,

196 Furthermore, N-acetylcysteine (NAC), an antioxidant and ROS scavenger,

197 odonium (DPI), a flavoenzyme inhibitor, or N-acetylcysteine (NAC), an antioxidant.

198 N-acetylcysteine (NAC), an FDA-approved anti-mucolytic age

199 The oxygen radical scavenger, N-acetylcysteine (NAC), attenuates the chemotoxicity of pl

200 nto four groups for daily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normoxia

201 stigate the effect of a thiol antioxidant, N-acetylcysteine (NAC), in SSc.

202 sly showed that the glutathione precursor, N-acetylcysteine (NAC), prevented hypoglycemia-associated

203 a total of 10 strategies: saline, statin, N-acetylcysteine (NAC), sodium bicarbonate (NaHCO3), NAC+N

204 ggest that the over-the-counter supplement N-acetylcysteine (NAC), via glutamate modulation in the nu

205 Treatment of cells with N-acetylcysteine (NAC), which sequesters ROS, prevents ant

206 d by the antioxidant L-cysteine derivative N-acetylcysteine (NAC).

207 ndow of the only current treatment option, N-acetylcysteine (NAC).

208 of ISO with the current standard of care, N-acetylcysteine (NAC).

209 lerance, and efficacy of the GSH precursor N-acetylcysteine (NAC).

210 N-Acetylcysteine (NAC, a clinically approved mucolytic dru

211 amples from 13 PALF survivors with APAPo + N-acetylcysteine (NAC, the frontline therapy for APAPo), 8

212 ions (corticosteroids, pentoxifylline, and N-acetylcysteine [NAC], alone or in combination) with each

213 As compared with placebo, acetylcysteine offered no significant benefit with respe

214 nt of CSE-knockout mice with NaHS, but not N-acetylcysteine or ezetimibe, inhibited the accelerated a

215 rast, reduction of adipose DNA damage with N-acetylcysteine or metformin ameliorated cellular senesce

216 ition of Th17 induction with ROS scavenger N-acetylcysteine or mitoquinone, a specific inhibitor for

217 duced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB inhibitor via down-regulatin

218 nous 0.9% sodium chloride and 5 days of oral acetylcysteine or oral placebo; of these patients, 4993

219 We focused on use of N-acetylcysteine or sodium bicarbonate for the prevention

220 N-Acetylcysteine or tris(2-carboxylethyl)phosphine as co-a

221 revented using reducing compounds, such as N-acetylcysteine or vitamin C, that enhance M. tuberculosi

222 lular level, the presence of antioxidants (N-acetylcysteine or vitamin E) significantly reduced the t

223 glutathione production with its precursor, N-acetylcysteine, or adding the reducing agent, dithiothre

224 Administration of an antioxidant chemical, N-acetylcysteine, or ectopically overexpressing a reactive

225 t microbiota, mice were aged, treated with N-acetylcysteine, or engineered to express the ROS scaveng

226 medication (serotonin reuptake inhibitors, N-acetylcysteine, or naltrexone).

227 over intravenous sodium chloride or of oral acetylcysteine over placebo for the prevention of death,

228 f RhoA-deficient mice with a ROS scavenger N-acetylcysteine partially restored thymocyte development.

229 They randomly received N-acetylcysteine, physiologic saline, or sodium bicarbonat

230 he greatest reduction in CIN was seen with N-acetylcysteine plus IV saline in patients receiving LOCM

231 ients receiving LOCM and with statins plus N-acetylcysteine plus IV saline.

232 However, N-acetylcysteine posttreatment worsened folic acid toxicit

233 Glutathione levels did not increase in N-acetylcysteine posttreatment.

234 Glutathione levels decreased less in N-acetylcysteine pretreatment but also increased beginning

235 The survival rates in N-acetylcysteine pretreatment mice were significantly bett

236 N-acetylcysteine pretreatment was effective in reducing th

237 Both CV-3988 and N-acetylcysteine reduced MS-WF-stimulated pneumococcal adh

238 Exposure to the antioxidant N-acetylcysteine reduced oxidative stress and improved sur

239 Treating mice in vivo with N-acetylcysteine reduces ROS levels, rescues HSC cycling d

240 red with 71 of 109 allocated to the standard acetylcysteine regimen (adjusted odds ratio 0.26, 97.5%

241 overdose to either the standard intravenous acetylcysteine regimen (duration 20.25 h) or a shorter (

242 with paracetamol poisoning, a 12 h modified acetylcysteine regimen resulted in less vomiting, fewer

243 ve patients assigned to the shorter modified acetylcysteine regimen versus 31 who were allocated to t

244 to confirm the efficacy of the 12 h modified acetylcysteine regimen.

245 We propose that N-acetylcysteine represents the first potential therapeuti

246 traperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte dev

247 urr1 in HEK293T cells, and the antioxidant N-acetylcysteine rescued from this effect.

248 ent of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to t

249 ways of BCR-derived ROS with the scavenger N-acetylcysteine resulted in impaired in vitro BCR-induced

250 tal treatment of mice with the antioxidant N-acetylcysteine reversed the pollutant-induced increased

251 The antioxidant N-acetylcysteine reversed this phenotype, reducing both ba

252 treated with vitamin E or sulforaphane and N-acetylcysteine; samples included A2E-free cells.

253 ld be reduced with either a shorter modified acetylcysteine schedule, antiemetic pretreatment, or bot

254 ion (statin therapy, acetylsalicylic acid, N-acetylcysteine, sodium bicarbonate, off-pump coronary re

255 Administration of N-acetylcysteine, sodium bicarbonate, or physiologic salin

256 N-acetylcysteine, sodium bicarbonate, statins, and ascorbi

257 I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species (R

258 t APAP-induced autophagy was suppressed by N-acetylcysteine, suggesting APAP mitochondrial protein bi

259 e intermediate formed a stable adduct with N-acetylcysteine, suggesting that oxidative transformation

260 ent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to th

261 he reactive oxygen species (ROS) scavenger N-acetylcysteine, suggesting that ROS contributes to magne

262 rsed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-medi

263 cell disease treated with the antioxidant N-acetylcysteine suggests that cysteine disulfides, in par

264 on and beta-oxidation products, as well as N-acetylcysteine, taurine and sulfo-conjugates in both rat

265 treated with the oxygen radical scavenger, N-acetylcysteine, the NKA inhibitory activity of plumbagin

266 nophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy.

267 lesions was abrogated by the anti-oxidant N-acetylcysteine, this treatment did not alter the accumul

268 Administration of N-acetylcysteine to control mice prevented VPA- and APAP-i

269 Fourteen healthy animals were given N-acetylcysteine to evaluate for toxicity and the other 24

270 fected murine macrophages, the addition of N-acetylcysteine to isoniazid treatment potentiated the ki

271 Addition of GSH or N-acetylcysteine to PBMCs selectively restored IL-12 and I

272 the PANORAMA study suggest that addition of acetylcysteine to pirfenidone does not substantially alt

273 cated that clinical benefit from addition of acetylcysteine to pirfenidone is unlikely, with the poss

274 e liver injury indicating need for continued acetylcysteine treatment beyond the standard course (ala

275 r CRH5 but not AB12, MM cells, and in vivo N-acetylcysteine treatment eliminated these effects.

276 Patients who needed intravenous acetylcysteine treatment for paracetamol overdose had ci

277 and May 29, 2014, 1187 patients who required acetylcysteine treatment for paracetamol overdose were r

278 N-acetylcysteine treatment resulted in significant reducti

279 In addition, the N-acetylcysteine treatment significantly increased BKCa ch

280 Compared with placebo, N-acetylcysteine treatment was associated with significant

281 tic injury" 20 hours following initiation of acetylcysteine treatment, defined as ALT doubling and pe

282 , 217 were assessable 2 h after the start of acetylcysteine treatment.

283 nd demonstrate beneficial effects of early N-acetylcysteine treatment.

284 cal trial of prednisone, azathioprine, and N-acetylcysteine underwent HRCT at study start and finish.

285 N-Acetylcysteine use was limited in this group, presumably

286 ain the variation from clinical studies of N-acetylcysteine use.

287 pretreatment with different antioxidants (N-acetylcysteine, vitamin E, or GSH ethyl ester) did not p

288 justed rate of decline 125.6 mL/6 months for acetylcysteine vs 34.3 mL/6 months for placebo; differen

289 e adverse event (46 [77%] patients receiving acetylcysteine vs 50 [81%] receiving placebo), adverse e

290 The trial continued as a two-group study (acetylcysteine vs. placebo) without other changes; 133 a

291 R-IPF, exposure to prednisone/azathioprine/N-acetylcysteine was associated with a higher composite en

292 n H(2)S-releasing compounds L-cysteine and N-acetylcysteine were added to the cell culture, the amoun

293 rs, nitroglycerin, diazepam, metoclopramide, acetylcysteine were associated with higher risk for AMI;

294 d EAAC1(-/-) mice chronically treated with N-acetylcysteine were evaluated at serial time points for

295 15 of the 32 participants (47%) receiving N-acetylcysteine were much or very much improved compared

296 bic acid, caffeic acid, chlorogenic acid and acetylcysteine were screened as antioxidant standards wi

297 re mitigated by the free radical scavenger N-acetylcysteine, which also reverted phagocytosis to base

298 dant and redox regulator compounds such as N-acetylcysteine, which could be used preventively in youn

299 rone 4-phenyl butyric acid and antioxidant N-acetylcysteine, which significantly attenuate lewisite-m

300 o interaction between sodium bicarbonate and acetylcysteine with respect to the primary end point (P=